Beside supraventricular extra beats, atrial fibrillation is the most common cardiac arrhythmia. Atrial fibrillation according to Douglas P. Zipes definition is an arrhythmia characterised by complete asynchronous atrial depolarisation, without following hemodynamic effective contraction. Atrial electric activity can be detected during electrocardiography as irregular oscillation of the isoelectric line of low and variable amplitude 350-600/min waves. Atrial fibrillation previously considered as a benign arrhythmia is associated with severe clinical complications as hemodynamic disturbances and closely connected with it cerebral embolization. In the present study we focused on left ventricle function during atrial fibrillation. We evaluate a deterious effect of high, irregular heart rate which stimulates left ventricle systolic dysfunction, so called "tachycardiomyopathy". Deterioration of left ventricle systolic function usually coexists with diastolic impairment, which is difficult to treat even if sinus rhythm is restored. We also analysed the pathophysiologic mechanism of left ventricle impairment during atrial fibrillation at cellular level. In second part of this paper we discussed dependence between size and function of left atrium and its appendage and atrial fibrillation induction. One must take into account of vicious circle mechanism induction during atrial fibrillation, which promotes arrhythmia stabilization, as well as after sinus rhythm restoration--may provoke recurrence of arrhythmia. Intracellular changes followed by electrophysiological alteration are regarded as causes of the mentioned mechanism. Accordingly to the newest studies, gene expression plays a role in arrhythmia induction and stabilization. This means that the problem is very complicated and also gives hope to effective treatment of atrial fibrillation including gene modification.